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Published on: April 16, 2019
IL-23 signaling enhances Th2 polarization and regulates allergic airway inflammation
Juan Peng1, Xuexian O Yang, Seon Hee Chang
1Department of Immunology, MD Anderson Cancer Center, Houston, TX 77030, USA.
Abstract:
IL-23/IL-17 axis is an important regulator in various inflammatory diseases. However, the role of IL-23 in allergic airway inflammation is not well understood. In this study, we show that in an allergen-induced asthma model, mice with transgenic overexpression of IL-23R exhibited increased airway infiltration of eosinophils and Th2 cytokine production, whereas those deficient in IL-23 displayed reduced airway inflammation. In vitro, IL-23-IL-23R signaling promoted GATA-3 expression and enhanced Th2 cytokine expression. Conversely, in the absence of this signal, Th2 cell differentiation was partially inhibited. Therefore, IL-23 signaling may regulate allergic asthma through modulation of Th2 cell differentiation.
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